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TCAP

● Preclinical
Teneurin C-Terminal Associated Peptide
Also known as: TCAP, Teneurin Peptide, Corticotropin-Inhibiting Peptide
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Quick Summary

Teneurin C-terminal associated peptide (TCAP) is a 40-41 amino acid bioactive peptide derived from the C-terminal region of the teneurin transmembrane proteins (teneurin-1 through -4). TCAPs are conserved from invertebrates to mammals and represent an ancient neuropeptide family.

Neuropeptide / Stress Regulation Preclinical
Teneurin C-terminal associated peptide (TCAP) is a 40-41 amino acid bioactive peptide derived from the C-terminal region of the teneurin transmembrane proteins (teneurin-1 through -4). TCAPs are conserved from invertebrates to mammals and represent an ancient neuropeptide family. In mammals, TCAP-1 modulates the stress response, reduces CRF-induced anxiety behaviors, promotes neuronal cytoskeletal organization, and has neuroprotective properties.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

Stress Axis Modulation

TCAP-1 reduces CRF receptor sensitivity and dampens CRF-induced HPA axis responses without directly antagonizing the CRF receptor. It activates beta-arrestin signaling pathways and downregulates CRF receptor surface expression through receptor internalization. This modulatory mechanism may allow TCAP to attenuate chronic stress responses without fully blocking the acute stress reaction.

Neuronal Cytoskeletal Effects

TCAP promotes neuronal process formation and stabilizes the actin cytoskeleton through interactions with dystroglycan complexes. In hippocampal neurons, TCAP treatment increases dendritic complexity and spine density. These structural effects may underlie its ability to improve cognitive resilience to stress and promote neuroplasticity.


Research Summary

Anxiety and PTSD Models

Preclinical

Repeated subcutaneous TCAP-1 administration reduces acoustic startle responses, contextual fear conditioning, and CRF-induced anxiety in rodents. Notably, TCAP-1 effects persist for weeks after the last injection, suggesting long-term neuroplastic changes. These properties support exploration in PTSD and anxiety disorder models.

Neuroprotection

Preclinical

TCAP-1 protects hippocampal neurons against ischemic and oxidative damage. It reduces reactive oxygen species, activates Nrf2/antioxidant pathways, and promotes mitochondrial integrity. The peptide also enhances glucose uptake in neurons through a dystroglycan-dependent mechanism, potentially improving neuronal metabolic resilience.


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Research Protocols

GoalDoseFrequencyRoute
Anxiety / PTSD model40 nmol/kg SCWeekly x 4 weeksSubcutaneous injection
Neuroprotection1-10 nMSingleCell culture / in vivo

Preclinical only. No human clinical data for TCAP peptides.


Interactions

Modulatory
CRF/CRH
TCAP downregulates CRF receptor sensitivity; dampens CRF signaling
Receptor
Dystroglycan
TCAP interacts with dystroglycan complexes for cytoskeletal effects
Downstream
Beta-1 integrin
TCAP activates integrin-linked kinase through dystroglycan

Safety Profile

TCAP-1 has an excellent preclinical safety profile with no observed adverse effects at effective doses in rodents. The prolonged behavioral effects from weekly dosing suggest tissue accumulation or long-lasting plasticity changes that require further characterization. No human pharmacokinetic or safety data available.


References

  • [1]Bhatt DL et al. (2012). Teneurin C-terminal associated peptide (TCAP) reduces distress and anxiety in rats. Psychoneuroendocrinology, 37(3), 353-363.
  • [2]Chand D et al. (2013). Biochemical and cell biological properties of the C-terminal region of teneurin-1. Biochemical Journal, 452(1), 63-73.
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Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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